Pregnancy has profound physiologic effects on a woman’s body, affecting not only the cardiovascular, endocrine, and renal systems,1 but also the musculoskeletal system, specifically the axial skeleton. Distinct hormonal changes accompanied by an increase in body mass and the presence of the gravid uterus cause a shift of the center of gravity, thereby exerting additional static and dynamic loads on the axial skeleton.
Recommended weight gain during pregnancy is 25 to 35 lb (11 to 16 kg), of which approximately half is gained in the abdomen.2 As a result, the enlarging abdomen (Figure 1) elicits postural compensations (Figure 2) that frequently culminate in the development of low back pain (LBP), the most common musculoskeletal complaint during pregnancy,3 and/or pelvic girdle pain (PGP). Gestational LBP typically begins in the second trimester, on average at 22 weeks of pregnancy. About half of women with initially manifesting LBP during pregnancy continue to have pain 1 year postpartum,4 and 20% are symptomatic 3 years after delivery.5 The prevalence of LBP during pregnancy ranges from 20% to 90%; most studies report a prevalence >50%.6,7 PGP typically begins by the end of the first trimester, peaking between the 24th and 36th gestational weeks; this usually resolves spontaneously within 6 months postpartum; however, in 8% to 10% of women, the pain continues for 1 year to 2 years postpartum.8,9 The incidence of PGP in pregnancy ranges from 4% to 76%, depending on the definition used, which often includes LBP. When defined as pain located from the level of the posterior iliac crest and the gluteal fold over the anterior and posterior elements of the bony pelvis, the prevalence has been reported as ranging from 16% to 25%.9 However, the precise definition of PGP often overlaps with that of LBP, inherently making all frequency indices obligatory estimates in the literature.
Considering the high incidence and prevalence of pregnancy-related LBP and PGP, this review specifically addresses these gestational musculoskeletal conditions, including their clinical differences, etiologies, diagnosis, and orthopaedic management.
Low Back Pain and Pelvic Girdle Pain in Pregnancy
Joint laxity increases during pregnancy10 as a result of increasing levels of relaxin, progesterone, and estrogen.11-13 Relaxin, a hormone produced by the corpus luteum and the placenta, increases from early pregnancy, peaks at the end of the first trimester, and then remains consistently elevated until late pregnancy.14 In one study, women experiencing the most incapacitating LBP had the highest amount of relaxin.15 Estrogen potentiates relaxin receptor sensitivity, thereby enhancing its effect on joints.12 Joint laxity is considered one of the etiologies of LBP and PGP in the pregnant patient. Unlike asymptomatic pregnant patients, pregnant women with moderate or severe posterior pelvic pain exhibit significant asymmetric sacroiliac joint laxity.16 Additionally, in women with pregnancy-related lumbopelvic pain, greater pubic symphysis mobility has been reported during pregnancy and puerperium compared with asymptomatic pregnant women.17 In many women, pregnancy-related joint pain is associated with increased concentrations of estradiol and progesterone;18 however, a definitive causative relationship has not been established.14,18
An enlarging gravid uterus stretches and weakens abdominal muscles, thereby placing additional strain on lumbar muscles that compensate for the loss of abdominal muscle tone and strength.12 Furthermore, the pelvis rotates sagittally about the second sacral segment, which acts as a fulcrum (Figure 3). Resultant compensatory hyperlordosis occurs as the gravid uterus causes the woman’s center of gravity to shift forward. This action creates an additional flexion moment on the lumbar spine that culminates in an increased load on the lumbar spinal musculature. In addition, anterior pelvic tilt increases as the center of gravity shifts anteriorly, causing a greater load through the sacroiliac ligaments as these structures attempt to resist this forward pelvic rotation. As the pregnancy progresses, these sacroiliac ligaments become lax and allow increased forward pelvic rotation and lumbar spine hyperlordosis, which subsequently place even more strain on the pelvis and low back3 (Figure 4). Axial loading of the spine, which causes compression of the intervertebral disks, may also contribute to LBP; excessive compression may result in the expulsion of fluid from the disks and decreased height.6 One study demonstrated that activity-related spinal compression is greater and post-activity recovery is longer in pregnant women with LBP compared with asymptomatic pregnant or nonpregnant women.19
Vascular changes may also contribute to back pain during pregnancy. The gravid uterus can place considerable compression on both the aorta and the vena cava when a woman is in the supine position. In addition to the potential risk of venous thromboembolism, the subsequent venous stasis and decreased regional oxygen saturation may lead to hypoxemia that compromises the metabolic activity of the neural structures, thereby causing LBP.12,20
Prevalence and Associated Factors
Lumbopelvic pain essentially encompasses three entities: (1) pregnancy-related LBP (herein referred to as LBP); (2) pregnancy-related PGP (herein referred to as PGP); and (3) combined pregnancy-related LBP and PGP.21 It usually begins around the 18th week of pregnancy and peaks between weeks 24 and 36.21 At 12 to 18 weeks’ gestation, the prevalence of lumbopelvic pain in pregnant patients was reported as 62%, with 33% experiencing PGP, 11% experiencing LBP, and 18% experiencing both.22 In another report, 50% of gestational lumbopelvic pain was caused by PGP, 33% by LBP, and 17% by both.21 Toward the end of pregnancy, at around 35 weeks, the prevalence of LBP and PGP were 71.3% and 64.7%, respectively.23 Strong predictors of lumbopelvic pain are strenuous work, previous lumbopelvic pain, and a history of pregnancy-related LBP or PGP.21 An increased incidence of LBP has been reported in pregnant women with advanced maternal age, a history of back pain during a previous pregnancy, increased parity, a higher body mass index, and a history of joint hypermobility.24,25 A history of back pain during a previous pregnancy is an especially strong predictor of experiencing back pain in subsequent pregnancies, with an 85% likelihood.6 Interestingly, there does not appear to be an association between LBP and maternal weight gain during pregnancy or the height or birth weight of the baby.24
In addition to the risk factors described earlier, previous pelvic trauma is also associated with the occurrence of PGP.26,27 Factors that do not appear to be associated with PGP include weight, height, age, and smoking.27 Pregnant patients with PGP are usually more disabled than those with LBP, exhibit much higher pain scores, and are more difficult to treat.8
Symptoms and Diagnosis
The differential diagnoses of LBP and PGP greatly overlap (Table 1), but a careful clinical history and physical examination can aid in making a definitive diagnosis5,9,28,29 (Table 2). Pregnancy-related PGP is usually experienced between the posterior iliac crest and the gluteal fold near one or both sacroiliac joints, occasionally radiating into the posterior thigh. It may occur in conjunction with or separately from the pubic symphysis, with possible radiation into the anterior thigh.27 Pain is intermittent, may be precipitated by prolonged sustained postures, and usually occurs within 30 minutes of common daily activities, such as walking, sitting, or standing.8 Pregnancy-related LBP is described as pain in the lumbar region, above the sacrum, and it may radiate into the leg. The pain is often dull and exacerbated by forward flexion. Spinal movement is often restricted in the lumbar region, while palpation of the erector spinae muscles intensifies symptoms.8 PGP can be clinically diagnosed and distinguished from LBP by several pain provocation tests (Table 3). These tests have high specificity and low sensitivity; therefore, it is recommended that all of these tests be performed whenever possible.8,27,29
Pregnancy-related posterior pelvic pain is defined as PGP without pubic symphysis pain, and making the clinical differentiation from LBP in pregnancy can be challenging. In contrast to LBP, posterior pelvic pain is characterized by a stabbing pain in the buttocks, distal and lateral to the area of L5 to S1; the pain may or may not radiate to the posterior thigh or knee. Posterior pelvic pain is often associated with weight bearing, the presence of pain-free intervals, normal range of motion at the hips and spine, no nerve root impingement, and a positive posterior pelvic pain provocation test.30
If symptoms are severe or are associated with neurologic compromise, further evaluation may be indicated. MRI is considered the safest and preferred imaging modality during pregnancy.6,8,9,28 Concerns have been raised by some clinicians regarding MRI-induced fetal teratogenicity, acoustic damage, and heating effects.31,32 However, current data have not demonstrated adverse effects following 1.5-T MRI exposure; the safety at 3-T exposure has not been thoroughly studied.31 Despite these findings, the International Commission on Non-Ionizing Radiation Protection recommends delaying elective MRI until after the first trimester because of potential risks.33 The American Congress of Obstetricians and Gynecologists (ACOG) states that during pregnancy, other imaging procedures not associated with ionizing radiation (eg, ultrasonography, MRI) should be considered instead of radiography, when appropriate,34 and notes that MRI has not been associated with known adverse fetal effects. Finally, the American College of Radiology 2013 guidelines recommend that MRI should be used in pregnant patients, regardless of gestational age, when the benefits outweigh the risks, even in the first trimester.35 Although studies regarding fetal risk with gadolinium contrast are lacking, most radiologists avoid its routine use in pregnancy.31
Unlike MRI, radiography uses ionizing radiation. The amount of radiation absorbed by the fetus depends on the gestational age; at 2 to 8 weeks, a dose of <10 cGy (ie, exposure equivalent to a three-view spine series) poses no significant risk for fetal abnormalities. The risk for anomalies increases 1% per 10-cGy increase.6 The fetus is most vulnerable at 8 to 15 weeks’ gestation, with ionizing radiation potentially leading to intrauterine growth retardation and central nervous system defects. With increasing radiation doses >100 mGy [10 cGy], spontaneous abortion is possible at 3 to 4 weeks’ gestation, and the risk of congenital malformation is increased if exposure occurs at 5 to 10 weeks’ gestation. Ionizing radiation also poses a carcinogenic risk. According to the International Commission on Radiological Protection, about 1 in 500 fetuses exposed to ≥30 mGy [3 cGy] of radiation will develop cancer.36
Fluoroscopy use during spinal surgery may place the fetus at significant risk and should be avoided whenever possible. If absolutely required for emergent or urgent surgical procedures, its risks can be minimized with proper uterine shielding and by reducing exposure time, collimating the beam width and exposure area, reducing image magnification, selecting appropriate radiation output, and using equipment that includes pulsed fluoroscopy and image storage-recall.31 In a simulation study, Theocharopoulos et al37 demonstrated that fluoroscopically guided spinal treatments exposed phantom fetuses lying outside the primary irradiated region to <4 mGy [0.4 cGy] during all gestational stages, incurring risks of cancer and congenital malformation that are lower than spontaneous incidence rates. However, when the phantom fetus was directly exposed to the fluoroscopy beam, the dose could reach as high as 105 mGy [10.5 cGy]. It was also determined in this simulation study that at least 35 minutes of fluoroscopy would be required to induce adverse fetal effects.
Although user-dependent, transvaginal/transperineal ultrasonography has been advocated in diagnosing and monitoring the progress of pubic symphysis pain and diastasis.9 Ultrasonography is also used for guided placement of epidural catheters in pregnant patients. Ultrasonography has no known significant risks to the fetus or the mother because tissue temperature increases would not be expected to exceed 32.9°F (0.5°C).31 Nonetheless, energy exposure has been arbitrarily restricted to 94 mW/cm2 by the FDA.36
CT is not recommended for evaluation of nontraumatic LBP or PGP but may be indicated when trauma is sustained in these regions. The estimated dose of a single pelvic CT during the first trimester is lower than the threshold dose at which fetal risk significantly increases, but the risk of childhood cancers may increase by a factor of two. The risk of adverse effects in the fetus is increased with multiphase CT studies and repeat scans. An increased risk of spontaneous abortion exists if the radiation dose is >0.1 Gy [10 cGy] within the first 2 weeks after conception, but there does not appear to be an increased risk thereafter.31
According to the European guidelines, issued by Working Group 4, MRI is the suggested imaging modality for evaluation of PGP in pregnant patients,27 whereas ACOG recommends use of MRI or ultrasonography when appropriate.34
Treatment of Pregnancy-related Low Back Pain and Pelvic Girdle Pain
Pennick and Liddle38 conducted a systematic review of 26 randomized, controlled trials that examined treatments for LBP, PGP, and combined LBP and PGP during pregnancy. For LBP, low-quality evidence showed that exercise significantly reduced pain and disability and that water exercise significantly reduced pain-related sick leave. The authors concluded that use of different support belts, exercise, neuro-emotional technique, and spinal manipulation had no significant effect on LBP and physical function. Low-quality evidence suggested that nocturnal pain may be better relieved by a specially designed pregnancy support pillow compared with a regular pillow.38 For PGP, moderate-quality evidence suggested that acupuncture more effectively reduced evening pain than did exercise, but both methods of management were more effective than the usual prenatal care alone. In a comparison of acupuncture with sham acupuncture, function and evening pain, but not the average pain score, were improved with acupuncture. Evening pain relief did not significantly differ between deep or superficial acupuncture. Low-quality evidence suggested that adding a rigid belt to exercise improves average pain but not function.38 For lumbopelvic pain, moderate-quality evidence showed that an 8- to 20-week exercise program reduced the risk for pain, but a 16- to 20-week training program was no more effective than the usual prenatal care. Low-quality evidence demonstrated that exercise significantly improved function and significantly reduced lumbopelvic pain-related sick leave. Pain and function were also significantly improved with osteopathic manipulation and with a combination of manual therapy, exercise, and education. Acupuncture improved pain and function better than did the usual prenatal care or physiotherapy and was more effective when started at 26 weeks’ gestation rather than at 20 weeks’ gestation. Ear acupuncture, compared with sham acupuncture, also significantly improved the outcomes.38
The safety of a medication during pregnancy is indicated by the category assigned to it by the FDA39 (Table 4). Acetaminophen in oral or rectal form is a category B drug that is the first-choice analgesic for mild back pain because it has no known teratogenic properties (intravenous form is category C). NSAIDs, such as ibuprofen and naproxen, are category C drugs in the first trimester (0 to 14 weeks) and the second trimester (14 to 28 weeks); in the third trimester (28 to 42 weeks), they are considered category D drugs because fetal risks have been demonstrated.39 The ductus arteriosus is essential for normal fetal circulation; however, the structure can close prematurely when NSAIDs are used at or near term and can lead to pulmonary hypertension.20 Therefore, use of NSAIDs during pregnancy should be short-term and restricted to the first and second trimesters. Full-dose aspirin is a category D drug throughout all three trimesters and has been associated with increased perinatal mortality, neonatal hemorrhage, decreased birth weight, prolonged gestation and labor, and possible birth defects.39 Low-dose aspirin can be used in pregnancy and is considered safe with respect to the risks of fetal malformation and major developmental impairment.
Cyclobenzaprine, a muscle relaxant, is an available category B medication that can be used in pregnancy, but methocarbamol, a category C drug, should be avoided if possible because its fetal risk has not been fully established.7 Opioids may be used for severe pain.20,40 Codeine, a category C drug, has been associated with respiratory malformations.40 The Collaborative Perinatal Project found no congenital anomalies associated with hydrocodone, meperidine, methadone, morphine, or oxycodone use during pregnancy. These drugs, along with fentanyl and hydromorphone, are rated as category B drugs.40 However, all opioid analgesics are rated as category D by the FDA if they are used for extended periods or in large doses near term. Therefore, opioid analgesics should not be administered near term and are strictly limited to short-term use.20,40
The use of epidural steroids during pregnancy is controversial even though a single dose appears to be of low risk to the fetus. Epidural steroids are best reserved for the pregnant patient who has the new onset of symptoms that are consistent with lumbar nerve root compression (ie, unilateral loss of deep tendon reflex, sensory/motor change in a dermatomal distribution).40 A recent review reported efficacy for the epidural analgesia treatment of PGP in pregnancy when delivered either in a single shot or as a temporary method of pain relief following extended administration during periods of increasing pain.9
The role of spine surgery for LBP and PGP in pregnancy is limited. When indicated, it requires careful coordination between the orthopaedic surgeon and the obstetrician; guidelines have been established in a study by Han et al.41 In the first trimester, the prone position may be used, whereas in the second trimester, the lateral decubitus position in either direction (depending on the direction of the lesion) is preferred. In the third trimester, the left lateral decubitus position should be used because of the risk of compression of the inferior vena cava with the right decubitus position. If the surgical field is located inferiorly in the left decubitus position and the patient is in the third trimester, the table can be tilted to assist in the surgical approach.41
After 34 weeks’ gestation, a decision should be made whether delivery is indicated prior to surgery. If there is progressive neurologic deficit at <34 weeks’ gestation, antenatal corticosteroids should be given, and decompression surgery should be planned in consultation with the obstetrician. In a truly urgent state, both procedures (ie, childbirth and spine surgery) can be performed under the same anesthesia. When antepartum surgery is considered, the patient should be advised of the risks and benefits to herself as well as to the fetus.41
Category B perioperative antibiotics (ie, ampicillin, cephalosporin) may be used prophylactically in the pregnant spinal patient. Epidural anesthesia is recommended for short surgical spine procedures, and general anesthesia is recommended for longer surgical spine procedures, such as fusions.41
Although there is no consensus, intraoperative fetal heart monitoring is not indicated before 20 weeks’ gestation; its indications are unclear between 20 and 23 weeks’ gestation. After 23 weeks’ gestation, however, intraoperative fetal heart monitoring is recommended for the detection of potential abnormalities, thus alerting the obstetrician to take urgent action to protect the fetus.41
Ideally, pain should not be a sole indication for surgery in patients with routine spinal disorders. However, surgery can be performed during pregnancy if the pain is incapacitating or refractory to conservative management measures, and/or if neurologic compromise is imminent.
Spondylolisthesis secondary to a defect in the pars interarticularis most commonly occurs at L5, which can subsequently translate or “slip” forward in relation to the end plate of S1. Degenerative spondylolisthesis, however, is a similar process that typically occurs at L4-L5 and is more common in women.3 In susceptible women, pregnancy may be a major independent factor for the development of degenerative spondylolisthesis. Sanderson and Fraser42 reported that multiparous women had a higher incidence of spondylolisthesis than did nulliparous women. Saraste43 determined that women with a previous diagnosis of spondylolisthesis did not experience an increase in LBP or vertebral body translation (ie, slippage) during pregnancy.
Lumbar Disk Herniation
Lumbar disk herniation occurs in about 1/10,000 pregnancies and typically presents with no symptoms or mild LBP. Pregnant patients experience similar symptoms to those of nonpregnant patients, including unilateral radiating leg pain and a positive straight leg raise test. Weinreb et al44 demonstrated that pregnancy alone does not confer a higher risk for lumbar disk herniation compared with nonpregnant women. Conservative, nonsurgical management is usually indicated for pregnant women with radiculopathy, with or without LBP; this treatment regimen includes rest, ice, physical therapy, lumbar support, analgesia, and/or muscle relaxants.30 MRI is the first and safest diagnostic test for pregnant women with persistent pain.45 Despite MRI findings, surgical treatment can be postponed until after delivery if the neurologic symptoms are minimal or stable. However, surgical intervention is warranted for women who experience bowel or bladder dysfunction or progressive motor weakness.
Less than 2% of patients with lumbar disk herniation progress to cauda equina syndrome, an urgent state that presents with radiating pain or numbness bilaterally in the legs, paralysis, and dysfunction of the bowel and bladder. Patients often have a positive straight leg raise test, reduced rectal sphincter tone, saddle anesthesia, and decreased deep tendon reflexes.7 MRI should be performed immediately in patients with these symptoms. Both cauda equina syndrome and progressive motor weakness are absolute indications for surgery, regardless of the stage of pregnancy. Although classic lumbar spine surgical methods include laminectomy and diskectomy, the more recent endoscopic diskectomy has emerged as a viable treatment option for debilitating disk herniation during pregnancy.7 Because the patient is positioned in reference to the microscope, endoscopic diskectomy obviates the need for general anesthesia, and the prone position avoids excessive abdominal compression.29
Pubic Symphysis Diastasis
Widening of the pubic symphysis occurs in pregnancy to accommodate descent of the fetal head through the birth canal; this process can begin as early as 8 to 10 weeks’ gestation and progress steadily throughout the pregnancy.45 Physiologic widening ≤10 mm is considered acceptable; this limited diastasis usually causes minimal or no symptoms.13 Increased risk for symptomatic diastasis is associated with multiparity, fetal macrosomia, precipitous labor, powerful uterine contractions, or previous pelvic pathology or trauma.30 Patients may experience a stinging pain around the pubic symphysis or sacroiliac joints that often radiates down their thighs. Stair climbing, walking, standing up, and carrying heavy objects may exacerbate the pain.30 Symptomatic diastasis that is <10 mm may be carefully observed or treated conservatively with a short course of anti-inflammatory drugs or with epidural analgesia. Treatment may also include an intrasymphyseal injection with hydrocortisone, chymotrypsin, and lidocaine once a day for 3 to 7 days. Activity modification, pelvic binders, and physical therapy may also be effective additions to the treatment regimen.30 Regardless of treatment, pubic symphysis widening begins to reverse shortly after delivery, with symptoms usually resolving by the eighth postpartum week, and the pubic symphysis normally returns to its baseline by 12 weeks postpartum.30,46
Frank rupture of the pubic symphysis is rare, with an incidence of 1 in 600 to 800 to 1 in 30,000 pregnancies.46 This condition is caused by the forceful descent of the fetal head against the pelvic ring during delivery.46 Suggested risk factors and/or associations include large fetal macrosomia, protracted labor, epidural analgesia, forceps delivery, shoulder dystocia, and maternal developmental hip dysplasia.46 A sudden pain is experienced in the region of the pubic symphysis and is often accompanied by an audible crack. Pain may radiate to the back or thighs, and a gap can be palpated at the symphysis along with abnormal hemipelvis mobility with lateral compression.20,46 If there is significant posterior tenderness at either sacroiliac joint, CT should be obtained to fully assess the extent of posterior ring involvement.46 Treatment should initially consist of bed rest in the lateral decubitus position and the use of a pelvic binder. Early partial weight-bearing mobilization with a walker (weight-bearing restrictions should be assigned to the same side as that with the sacroiliac pain) and periodic follow-up radiographs should be obtained to confirm symphysis and sacroiliac joint closures46,47 (Figure 5). Surgical intervention should be reserved for open pubic symphysis rupture secondary to vaginal tearing, diastasis with the pelvic binder in place, or symptomatic diastasis refractory to conservative management, or if one or both of the sacroiliac joints are displaced, suggesting pelvic instability.46 Surgical options may include pubic symphysis open reduction and internal fixation with plates and screws or external fixation of the pelvis, followed by reduction and percutaneous iliosacral screws if the sacroiliac joints remain widened and unstable.30,46
Although the natural musculoskeletal changes accompanying pregnancy vary from woman to woman, LBP and PGP will be a problem for some patients. Because the most significant and noticeable physical change occurs in the abdominal region with the growing gravid uterus, it is not unexpected that the lumbar spine and the pelvic region are most affected. It is important for the patient and the physician to be aware of these effects in order to recognize symptoms that are outside those considered normal for pregnancy because some conditions can have lasting, debilitating consequences. Equally important is that orthopaedic surgeons recognize the musculoskeletal conditions that may arise during pregnancy so that appropriate and early treatment may begin to minimize a patient’s symptoms and, with certain conditions, prevent long-term sequelae.
Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, references 4, 5, 10, 18, 19, 22, 23, and 44 are level II studies. References 14-17, 24, 25, and 45 are level III studies. References 32, 37, 38, 41, 42, and 47 are level IV studies. References 1-3, 6-9, 11-13, 20, 21, 26-31, 33-36, 39, 40, 43, and 46 are level V expert opinion.
References printed in bold type are those published within the past 5 years.
1. Alden KR, Lowdermilk DL, Cashion MC, Perry SE: Anatomy and physiology of pregnancy
, in Maternity and Women’s Health Care. St. Louis, MO,Mosby, 2012, pp 296–301.
2. Chapman L, Durham R: Antepartal period, in Maternal-Newborn Nursing: The Critical Components of Nursing Care, ed 1
. Philadelphia, PA, FA Davis Company, 2009, p 74.
3. Ritchie JR: Orthopedic considerations during pregnancy
. Clin Obstet Gynecol 2003;46(2):456–466.
4. Padua L, Caliandro P, Aprile I, et al.: Back pain in pregnancy
: 1-year follow-up of untreated cases. Eur Spine J 2005;14(2):151–154.
5. Norén L, Östgaard S, Johansson G, Östgaard HC: Lumbar back and posterior pelvic pain during pregnancy
: A 3-year follow-up. Eur Spine J 2002;11(3):267–271.
6. Sabino J, Grauer JN: Pregnancy
and low back pain
. Curr Rev Musculoskelet Med 2008;1(2):137–141.
7. Han IH: Pregnancy
and spinal problems. Curr Opin Obstet Gynecol 2010;22(6):477–481.
8. Vermani E, Mittal R, Weeks A: Pelvic girdle pain
and low back pain
: A review. Pain Pract 2010;10(1):60–71.
9. Kanakaris NK, Roberts CS, Giannoudis PV: Pregnancy
-related pelvic girdle pain
: An update. BMC Med 2011;9:15.
10. Schauberger CW, Rooney BL, Goldsmith L, Shenton D, Silva PD, Schaper A: Peripheral joint laxity increases in pregnancy
but does not correlate with serum relaxin levels. Am J Obstet Gynecol 1996;174(2):667–671.
11. Beckmann CR, Ling FW, Barzansky BM, Herbert WN, Laube DW, Smith RP: Maternal-fetal physiology, in Obstetrics and Gynecology, ed 6
. Philadelphia, PA, Wolters Kluwer/Lippincott Williams & Wilkins, 2010, p 50.
12. Sneag DB, Bendo JA: Pregnancy
-related low back pain
. Orthopedics 2007;30(10):839–845.
13. Ireland ML, Ott SM: The effects of pregnancy
on the musculoskeletal system. Clin Orthop Relat Res 2000;372:169–179.
14. Aldabe D, Ribeiro DC, Milosavljevic S, Dawn Bussey M: Pregnancy
-related pelvic girdle pain
and its relationship with relaxin levels during pregnancy
: A systematic review. Eur Spine J 2012;21(9):1769–1776.
15. MacLennan AH, Nicolson R, Green RC, Bath M: Serum relaxin and pelvic pain of pregnancy
. Lancet 1986;328(8501):243–245.
16. Damen L, Buyruk HM, Güler-Uysal F, Lotgering FK, Snijders CJ, Stam HJ: Pelvic pain during pregnancy
is associated with asymmetric laxity of the sacroiliac joints. Acta Obstet Gynecol Scand 2001;80(11):1019–1024.
17. Mens JM, Pool-Goudzwaard A, Stam HJ: Mobility of the pelvic joints in pregnancy
-related lumbopelvic pain
: A systematic review. Obstet Gynecol Surv 2009;64(3):200–208.
18. Marnach ML, Ramin KD, Ramsey PS, Song SW, Stensland JJ, An KN: Characterization of the relationship between joint laxity and maternal hormones in pregnancy
. Obstet Gynecol 2003;101(2):331–335.
19. Rodacki CL, Fowler NE, Rodacki AL, Birch K: Stature loss and recovery in pregnant women with and without low back pain
. Arch Phys Med Rehabil 2003;84(4):507–512.
20. Borg-Stein J, Dugan SA, Gruber J: Musculoskeletal aspects of pregnancy
. Am J Phys Med Rehabil 2005;84(3):180–192.
21. Wu WH, Meijer OG, Uegaki K, et al.: Pregnancy
-related pelvic girdle pain
(PPP), I: Terminology, clinical presentation, and prevalence. Eur Spine J 2004;13(7):575–589.
22. Gutke A, Östgaard HC, Öberg B: Predicting persistent pregnancy
-related low back pain
. Spine (Phila Pa 1976) 2008;33(12):E386–E393.
23. Kovacs FM, Garcia E, Royuela A, González L, Abraira V; Spanish Back Pain Research Network: Prevalence and factors associated with low back pain
and pelvic girdle pain
: A multicenter study conducted in the Spanish National Health Service. Spine (Phila Pa 1976) 2012;37(17):1516–1533.
24. Mantle MJ, Greenwood RM, Currey HL: Backache in pregnancy
. Rheumatol Rehabil 1977;16(2):95–101.
25. Mogren IM, Pohjanen AI: Low back pain
and pelvic pain during pregnancy
: Prevalence and risk factors. Spine (Phila Pa 1976) 2005;30(8):983–991.
26. Bastiaanssen JM, de Bie RA, Bastiaenen CH, Essed GG, van den Brandt PA: A historical perspective on pregnancy
-related low back and/or pelvic girdle pain
. Eur J Obstet Gynecol Reprod Biol 2005;120(1):3–14.
27. Vleeming A, Albert HB, Östgaard HC, Sturesson B, Stuge B: European guidelines for the diagnosis and treatment of pelvic girdle pain
. Eur Spine J 2008;17(6):794–819.
28. Noon ML, Hoch AZ: Challenges of the pregnant athlete and low back pain
. Curr Sports Med Rep 2012;11(1):43–48.
29. Bhardwaj A, Nagandla K: Musculoskeletal symptoms and orthopaedic complications in pregnancy
: Pathophysiology, diagnostic approaches and modern management. Postgrad Med J 2014;90(1066):450–460.
30. Smith MW, Marcus PS, Wurtz LD: Orthopedic issues in pregnancy
. Obstet Gynecol Surv 2008;63(2):103–111.
31. Baysinger CL: Imaging during pregnancy
. Anesth Analg 2010;110(3):863–867.
32. Wang PI, Chong ST, Kielar AZ, et al.: Imaging of pregnant and lactating patients: Part 1, evidence-based review and recommendations. AJR Am J Roentgenol 2012;198(4):778–784.
33. International Commission on Non-Ionizing Radiation Protection: Medical magnetic resonance (MR) procedures: Protection of patients. Health Phys 2004;87(2):197–216.
34. ACOG Committee on Obstetric Practice: ACOG Committee Opinion.Number 299, September 2004 (replaces No. 158, September 1995). Guidelines for diagnostic imaging during pregnancy
. Obstet Gynecol 2004;104(3):647–651.
35. Kanal E, Barkovich AJ, Bell C, et al.; Expert Panel on MR Safety: ACR guidance document on MR safe practices: 2013. J Magn Reson Imaging 2013;37(3):501–530.
36. Khandelwal A, Fasih N, Kielar A: Imaging of acute abdomen in pregnancy
. Radiol Clin North Am 2013;51(6):1005–1022.
37. Theocharopoulos N, Damilakis J, Perisinakis K, Papadokostakis G, Hadjipavlou A, Gourtsoyiannis N: Fluoroscopically assisted surgical treatments of spinal disorders: Conceptus radiation doses and risks. Spine (Phila Pa 1976) 2006;31(2):239–244.
38. Pennick V, Liddle SD: Interventions for preventing and treating pelvic and back pain in pregnancy
. Cochrane Database Syst Rev 2013;8:CD001139.
39. Black RA, Hill DA: Over-the-counter medications in pregnancy
. Am Fam Physician 2003;67(12):2517–2524.
40. Rathmell JP, Viscomi CM, Ashburn MA: Management of nonobstetric pain during pregnancy
and lactation. Anesth Analg 1997;85(5):1074–1087.
41. Han IH, Kuh SU, Kim JH, et al.: Clinical approach and surgical strategy for spinal diseases in pregnant women: A report of ten cases. Spine (Phila Pa 1976) 2008;33(17):E614–E619.
42. Sanderson PL, Fraser RD: The influence of pregnancy
on the development of degenerative spondylolisthesis. J Bone Joint Surg Br 1996;78(6):951–954.
43. Saraste H: Spondylolysis and pregnancy
—a risk analysis. Acta Obstet Gynecol Scand 1986;65(7):727–729.
44. Weinreb JC, Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR: Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology 1989;170(1):125–128.
45. Becker I, Woodley SJ, Stringer MD: The adult human pubic symphysis: A systematic review. J Anat 2010;217(5):475–487.
46. Amorosa LF, Amorosa JH, Wellman DS, Lorich DG, Helfet DL: Management of pelvic injuries in pregnancy
. Orthop Clin North Am 2013;44(3):301–315.
47. Jain N, Sternberg LB: Symphyseal separation. Obstet Gynecol 2005;105(5 Pt 2):1229–1232.